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The disease onset and life span of SOD1\u2010G93A mice were recorded. Motor neurons (MNs) in anterior horn of spinal cord were quantified by Nissl staining and SMI\u201032 immunostaining. Hematoxylin and eosin (H&amp;E), nicotinamide adenine dinucleotide hydrogen (NADH), modified Gomori trichrome (MGT), and \u03b1\u2010bungarotoxin\u2010ATTO\u2010488 staining were also performed to evaluate muscle and neuromuscular junction (NMJ) damage. Expressions of aggregated SOD1 protein and autophagy\u2010related proteins were further detected by Western blot and immunofluorescent staining.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Carbamazepine treatment could delay the disease onset and extend life span of SOD1\u2010G93A mice by about 14.5% and 13.9%, respectively. Furthermore, CBZ treatment reduced MNs loss by about 46.6% and ameliorated the altered muscle morphology and NMJ. Much more interestingly, mechanism study revealed that CBZ treatment activated autophagy via AMPK\u2010ULK1 pathway and promoted the clearance of mutant SOD1 aggregation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings uncovered the therapeutic effects of CBZ against disease pathogenesis in SOD1\u2010G93A mice, indicating a promising clinical utilization of CBZ in ALS therapy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12855","type":"journal-article","created":{"date-parts":[[2018,4,15]],"date-time":"2018-04-15T05:21:30Z","timestamp":1523769690000},"page":"1163-1174","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Repurposing carbamazepine for the treatment of amyotrophic lateral sclerosis in SOD1\u2010G93A mouse 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